Stat5 is required for IL-2-induced cell cycle progression of peripheral T cells. Immunity 1999 Feb;10(2):249-59
Date
03/11/1999Pubmed ID
10072077DOI
10.1016/s1074-7613(00)80025-4Scopus ID
2-s2.0-0033082138 (requires institutional sign-in at Scopus site) 496 CitationsAbstract
Many cytokines activate two highly homologous Stat proteins, 5a and 5b. Mice deficient in both genes lack all growth hormone and prolactin functions but retain functions associated with cytokines such as erythropoietin. Here, we demonstrate that, while lymphoid development is normal, Stat5a/b mutant peripheral T cells are profoundly deficient in proliferation and fail to undergo cell cycle progression or to express genes controlling cell cycle progression. In addition, the mice lack NK cells, develop splenomegaly, and have T cells with an activated phenotype, phenotypes seen in IL-2 receptor beta chain-deficient mice. These phenotypes are not seen in mice lacking Stat5a or Stat5b alone. The results demonstrate that the Stat5 proteins, redundantly, are essential mediators of IL-2 signaling in T cells.
Author List
Moriggl R, Topham DJ, Teglund S, Sexl V, McKay C, Wang D, Hoffmeyer A, van Deursen J, Sangster MY, Bunting KD, Grosveld GC, Ihle JNAuthor
Demin Wang PhD Professor in the Microbiology and Immunology department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AnimalsCell Cycle
Cell Division
Cells, Cultured
DNA-Binding Proteins
Flow Cytometry
Interleukin-2
Mice
Mice, Mutant Strains
Milk Proteins
STAT5 Transcription Factor
T-Lymphocytes
Thymus Gland
Trans-Activators
